"Dear Steve, I saw a patient this morning with your book [in hand] and highlights throughout. She loves it and finds it very useful to help her in dealing with atrial fibrillation."

Dr. Wilber Su Cavanaugh Heart Center, Phoenix, AZ

"Your book [Beat Your A-Fib] is the quintessential most important guide not only for the individual experiencing atrial fibrillation and his family, but also for primary physicians, and cardiologists."

"Steve Ryan's summaries of the Boston A-Fib Symposium are terrific. Steve has the ability to synthesize and communicate accurately in clear and simple terms the essence of complex subjects. This is an exceptional skill and a great service to patients with atrial fibrillation."

Dr. Jeremy Ruskin of Mass. General Hospital and Harvard Medical School

"Steve, your website was so helpful. Thank you! After two ablations I am now A-fib free. You are a great help to a lot of people, keep up the good work."

Terry Traver, former A-Fib patient

"If you want to do some research on AF go to A-Fib.com by Steve Ryan, this site was a big help to me, and helped me be free of AF."

Roy Salmon Patient, A-Fib Free; pacemakerclub.com, Sept. 2013

Drug Therapies for A-Fib patients

Medicines or ‘Drug Therapies’ for Treatment of A-Fib

The various medications, or drugs, for treatment of Atrial Fibrillation can be overwhelming. What they are for, how they work and how they might affect you can be confusing. We’ll give you a basic understanding of the various ‘drug therapies’ you may be prescribed, so that you can become an intelligent participant in your own healing process.

A Two-Pronged Approach

Drug therapy treatment of Atrial Fibrillation is a two-pronged approach:

• Drug therapy for management of increased risk of clots and stroke: Anticoagulants (blood thinners) are used to reduce the risk of stroke.

• Drug therapies for management of Atrial Fibrillation: Rate Control drugs and Rhythm control (Antiarrhythmic) drugs are two approaches designed to control the heart rate (rate control), or to regain and maintain normal heart rhythm (antiarrhythmics).

Word of Caution

Always be cautious when taking prescription medications. “Adverse effects of medications are the fourth-leading cause of death in the US (after heart disease, cancer and stroke).”1 In an average year, there are roughly 200,000 deaths and over 500,000 adverse events reported due to prescription drugs.2

Sir William Osler, first chief of medicine of the most prestigious medical school in the world, Johns Hopkins, and considered to be the father of modern medicine because of his methodical, scientifically based approach, made this sobering warning, “One of the first duties of the physician is to educate the masses not to take medicine.”3

Medicines, by definition, are almost all unnatural. Medications are not like taking vitamins. They need to be taken with caution. Our bodies see medications as toxins and try to eliminate or clear them. But if one has A-Fib, medications may sometimes offer hope of stopping A-Fib or making it more bearable.

In general, don’t expect miracles from current medications. To date, the magic pill that will cure your A-Fib probably doesn’t exist.4 “Drugs don’t cure A-Fib but merely keep it at bay.”5

A-Fib creates an increased risk of Stroke

Treatment for stroke Risk

Blood Thinners

Blood thinners are used to prevent blood clots and stroke (anticoagulants like warfarin, Coumadin, Jantoven; antiplatelets like Aspirin, Ecotrin, Plavix, Ticlid); or Lovenox (an anticoagulant taken by injection), and Heparin (used in hospitalized patients. (Plavix and Ticlid are antiplatelet drugs like aspirin but they are not the same or interchangeable with aspirin. If your doctor prescribes Plavix or Ticlid, you should not substitute aspirin for them.)

But blood thinners are not like taking vitamins. They have their own set of risks and side effects. However, preventing a stroke is for most people a welcome trade-off for any bad effects of anticoagulants.

Blood thinners reduce but do not totally eliminate the risk of stroke.

To be effective warfarin must be maintained at a certain level in the blood stream (INR—International Normalized Ratio between 2.0 and 3.0). Above 4.0 you run the risk of having a hemorrhagic (bleeding) stroke. Below 2.0 you are more in danger of having an ischemic (clotting) stroke, the kind that most often occurs in A-Fib.

VIDEO:Stroke Prevention in A-Fib and Anticoagulant Therapy.Through interviews and animations, explains how atrial fibrillation can cause stroke and why anticoagulation is so important; Discussion of: warfarin (generic name), the required [monthly] monitoring, interactions with food, alcohol and other drugs: newer anticoagulants do not required regular testing.

It is often difficult to maintain this INR, especially when you first start on warfarin. You may have to take sometimes weekly PT tests in your doctor’s office till you get the warfarin dosage and INR right. There are home use kits available for testing your own INR (for example, see http://www.PTINR.com}.

In general, aspirin is less effective than warfarin.6 (For more, see FAQs questions #6 Which is better—warfarin or aspirin? Be advised that aspirin therapy can be dangerous for otherwise healthy people, “Regular aspirin therapy use in healthy people increased the occurrence of serious internal bleeding by 31%, but had no significant effect on fatal heart attack or any kind of stroke.” 7

You should also get tested for variations in the CYP2C9 and VKORC1 genes which influence how you respond to warfarin (Coumadin). If your doctor doesn’t provide this testing, you may want to think about getting a second opinion. These tests could save you heart problems related to over- and under-dosing of warfarin.

Removing or closing off the Left Atrial Appendage (LAA) may affect how well the heart pumps and is of special concern to athletes and to those with heart pumping problems. In canine studies the LAA provided 17.2% of the whole left atrial volume of blood pumped.8 It’s possible that removing or closing off the LAA may lead to heart pumping problems. The LAA is like a surge tank on a hot water heater. When the Mitral Valve closes, the LAA absorbs the surge of blood. When the LAA is amputated or closed off, this may cause increased pressure in the Pulmonary Veins and exercise intolerance. Few, if any, centers currently perform pre- and post-amputation exercise testing.

The New Oral Anticoagulants (NOACs)

The FDA has approved several new blood thinners—dabigatran (brand name Pradaxa), rivaroxaban (Xarelto), and apixaban (Eliquis) which are considered as effective or even more effective than warfarin without many of the accompanying problems of warfarin.

New Anticoagulants

Dabigatran (brand name Pradaxa) is a direct thrombin inhibitor, a newer type of medication. Thrombin is an enzyme that converts soluble fibrinogen into insoluble fibrin. Fibrin is a fibrous protein involved in the clotting of blood. It forms a mesh or clot over a wound.

Another new anticoagulant approved by the FDA Nov. 4, 2011 is rivaroxaban (Xarelto) which may work better for some patients than dabigatran. It is in a class of medications called Xa inhibitors (xabans). The FDA has approved another new anticoagulant apixaban (Eliquis) approved December 2012. “the results of large randomized trials indicate that bleeding remains a major concern even with the new agents. Studies with rivaroxaban, edoxaban and dabigatran showed that these drugs have incidences of severe bleeding comparable to those of enoxaparin and warfarin.”9

Drug Therapies for A-Fib

There are two basic approaches to managing Atrial Fibrillation with medications: Rate Control drugs and Rhythm Control drugs.

Rate Control drugs try to control the heart rate (ventricular beats), but leave the heart in A-Fib. 10 Rhythm control drugs try to stop the A-Fib and make your heart beat in normal rhythm by using antiarrhythmic drugs.

Approach 1: Rate Control

Rate control drugs aren’t really a “treatment” for A-Fib. Though they slow the rate of the ventricles, they leave you in A-Fib. They may alleviate some A-Fib symptoms, but do not address the primary risks of stroke and death associated with A-Fib.11

About drug therapies

Keep in Mind: Leaving patients in A-Fib overworks the heart and leads to remodeling and fibrosis which increase the risk of stroke.12 Mellanie True Hills of StopAfib.org asks, “Should we leave folks in A-Fib long term, especially the non-elderly? Between the risk of heart failure, and fibrosis from long-term remodeling increasing stroke risk, could staying in A-Fib long-term be a death sentence?”13 If your doctors only prescribe rate control meds for your A-Fib, you should question them and probably get a second opinion.

Categories of Rate Control Medications

Medications used for rate control can be categorized as:

Calcium-channel blockers

Beta-blockers

Cardiac Glycosides

1. Calcium channel blockers prevent or slow the flow of calcium ions into smooth muscle cells such as the heart and blood vessels. Calcium channel blockers are preferred if you have heart or lung disease. Common side effects are the heart beats too slowly, constipation, low blood pressure and heart failure.14“Calcium channel blockers weaken the heart and can damage the liver,” according to Dr. Julian Whitaker in his Health & Healing newsletter of October 2015.

Update 9/15/14:A study of nearly 3,000 women found that “women who took calcium-channel blockers for 10 years or longer had more than double the risk for breast cancer.” No risk was found for short-term use (less than 10 years).15Calcium-channel blockers include: diltiazem (Dilt, Cardizem, Tilazem, Cartia XT) [the generic name of a medication is listed first, the Brand name is in parentheses] and verapamil (Calan, Isoptin).

2. Beta-blockers “block” the action of adrenaline on beta receptors in the cells of heart muscle. They slow down conduction through the heart and make the AV Node less sensitive to A-Fib impulses.

Beta-blockers are better for active or young people, because exercise reduces the effectiveness of Digitalis and Calcium-channel blockers.

Common side effects are: the heart beats too slowly, low blood pressure, tiredness, and loss of sex-drive.16,17In many people, beta-blockers can reduce heart rate by 10 to 30 beats per minute.18Beta-blockers like metoprolol can be particularly dangerous for older people (over 60) and cause symptoms similar to aging,19Beta blockers also carry substantial risk for psychiatric side effects, particularly depression. When using beta blockers, a person’s psychiatric health should be monitored carefully.20“Beta-blockers are notorious for causing impotence, fatigue, and depression,” according to Dr. Julian Whitaker in his Health & Healing newsletter of October 2015.

Note: A new study casts doubt on the effectiveness of most beta-blockers, because they promote fibrosis in the heart.

Beta-blockers “undermine the structure and function of the heart…Blocking the beta-receptor alone promotes cardiac remodeling via growth of cardiac fibroblasts induced by alpha-adrenergic receptor signaling. The growth of fibroblasts in the heart further damages the integrity and function of the heart.”) 21

Carvedilo (Coreg)l, however, targets both the beta- and alpha-adrenergic receptors on the heart muscle. “Beta-blockers (like carvedilol) which target both receptors “offer the most benefit to cardiac patients.” A study in 2003 showed that carvedilol produced a greater survival rate than metoprolol. (Thanks to Janet Brown for calling our attention to this research.)

Nebivolol seems to eliminate most of the common bad side effects of beta blockers by dilating blood vessels through the release of nitric oxide. But it also only blocks Beta 1 receptors.

3. Cardiac Glycosides slow down and control the heart rate by blocking the electrical conduction between the atria and ventricles. The most widely prescribed Glycoside is digoxin (a Digitalis compound, brand names Lanoxin, Digitek), but medical authorities consider it the least effective.22

While Digoxin is the most commonly used drug for rate control, it is only effective at controlling heart rate at rest, i.e., when you are in the doctor’s office. But when you leave, your heart rate may go too high. It’s not as effective at controlling heart rate during physical activity or when stressed (when the sympathetic nervous system is more active). Beta-blockers and calcium-channel blockers are generally more effective than Digoxin.23

Caveat about digoxin: A 2013 study found that A-Fib patients “taking the heart drug digoxin were 35% more likely to suffer a cardiovascular-related death and 61% more likely to die due to an arrhythmia (irregular heartbeat) than A-Fib patients not taking digoxin.”

If you’re taking digoxin, talk to your doctor about switching to beta-blockers or calcium channel blockers to slow down fast heart rate. If you and your doctor conclude digoxin is the best drug for you, try to use the lowest possible dose and make sure you are closely monitored. 24

If using rate control drugs, be advised that you will still have A-Fib.

About All Rate Control Drugs

If you are using any of the above rate control drugs, please be advised that you will still have A-Fib. Only your lower heart (the ventricles) is controlled. You are still at risk of stroke and must continue taking blood thinners.

Approach 2: Rhythm Control

Rhythm control medications called anti-arrhythmic drugs have been available for nearly 100 years and remain a mainstay in the management of atrial fibrillation. These drugs target a reduction in the frequency and duration of episodes of arrhythmia.

Many antiarrhythmic drugs require you to be hospitalized for 3-4 days when they are initially administered, in order to monitor you for bad side effects. Some antiarrhythmic meds can have a “pro-arrhythmic” effect on some people (people react differently to medications).

About drug therapies

Keep in Mind: In general current “antiarrhythmic” (anti irregular heart rhythm) drugs aren’t always effective and tend to have bad side effects such as pulmonary fibrosis and impaired liver function.25‘26‘27‘28They also become less effective over time, with approximately half of the patients eventually developing resistance to them.29Up-to 50% of patients experience a recurrence of A-Fib after 1-year of antiarrhythmic treatment, and up-to 85% experience a recurrence after 2-years.30‘31

According to Drs. Savelieva and Camm, “The plethora of antiarrhythmic drugs currently available for the treatment of A-Fib is a reflection that none is wholly satisfactory, each having limited efficacy combined with poor safety and tolerability.”32

Classes of Antiarrhythmic Drugs

Antiarrhythmic drugs are grouped in “classes” according to how they work:

1. Class I are Sodium Channel Blockers which decrease the speed of electrical conduction in the heart muscle.

2. Class II are Beta-Adrenergic or Beta-Blockers which slow down conduction through the heart and make the AV node less sensitive to A-Fib impulses.

4. Class IV are Calcium Channel Blockers which prevent or slow the flow of calcium ions into smooth muscle cells such as the heart. This impedes muscle cell contraction, thereby allowing blood vessels to expand and carry more blood and oxygen to tissues.

Here is a list of the more commonly used antiarrhythmic drugs, based on an article by Dr. R. Falk of the Boston University School of Medicine: 33

Procainamide (Procan SR, Promine, Pronestyl, Procanbid): Slows nerve impulses in the heart and reduces the sensitivity of heart tissue. Not FDA approved for A-Fib. Long-term use associated with lupus. Generally not used as a first-time drug because of bad side effects. Less effective against A-Fib than the other Class 1A drugs Quinidine and Disopyramide.34 (Class 1A drug)

Quinidine (Quinaglute, Quinidine Glaconate, Quinidex): FDA approved for A-Fib but risk of death increases during long-term use. Generally not used as a first-time drug because of bad side effects such as increasing the heart rate and impairing the heart’s pumping efficiency. (Class 1A drug)

Disopyramide (Norpace): Not FDA approved for A-Fib. Strong negative inotropic effect (heart muscle contractions weakened). Generally not used as a first-time drug. Good for patients with nocturnal or post-prandial (after meals) A-Fib.35

Flecainide (Tambocor): Slows nerve impulses in the heart and makes the heart tissue less sensitive. Approved only for paroxysmal (occasional) A-Fib with structurally normal heart. Normally the first drug tried on otherwise healthy patients with new A-Fib. Not recommended after a heart attack or if you have a structural heart disease. (Class 1C drug)

Propafenone (Rhythmol and the newer version Rhythmol SR): Same limitations as flecainide. (Class 1C drug)

Sotalol (Betapace): Not recommended (conversion from A-Fib to normal rhythm rate is low). Only approved in the US for ventricular arrhythmias. (Class II and class III drug—a beta-blocker with antiarrhythmic effects). Should not be used in patients with severe heart failure or those with a long QT interval (see my article: Understanding the EKG Signal), because it may trigger a lethal cardiac arrhythmia in those patients. May cause severe fatigue.36

Dofetilide (Tikosyn): FDA-approved for conversion and maintenance. (Class III drug). Patients starting this medication must be monitored in a hospital for three days.

Amiodarone (Cordarone, Pacerone): Not FDA-approved for A-Fib. Moderately effective for conversion from A-Fib to normal rhythm, but onset is slow. Good rate slowing in A-Fib. This is usually the last drug tried on patients because of its toxic side effects particularly in the lungs, thyroid, and liver. (Class III drug but it also blocks Sodium Channels like a Class I drug.)

Dronedarone (Multaq): FDA approved in 2009. Chemically similar to amiodarone. While not as effective as amiodarone, it has less toxic side effects. Not for patients with severe heart failure.

Ibutilide (Corvert): Not for patients with low blood potassium, a prolonged QT interval (slow heart beat), or torsade de pointes (very irregular, fast ventricular heart beats). Effective in electrical cardioversion. Often used in place of Electrocardioversion (33% to 49% success rate) and is generally more effective in cases of Atrial Flutter than in A-Fib. (Class III drug)

The Class 1 drugs Quinidine, Procainamide, Disopyramide, Flecainide, and Propafenone should probably be avoided if you’ve had a heart attack or have structural heart disease. The Class III drugs Amiodarone, Sotatol, Dofetilide, and Azimilide appear to be safer to use if you have structural heart disease.37 In structurally normal hearts, Class IC drugs (Flecainide and Propafenone) cause less heart rhythm problems and are the least toxic.38

Xanax (alprazolam): Xanax does seem to have beta-blocker properties, though it is primarily used to help panic attacks. But be advised that Xanax is a controlled substance and might be addictive. Sally writes that her A-Fib comes on at night and is very severe, preventing her from sleeping. “I get up and take Xanax .05 mg, and within 15 minutes or so, the A-Fib stops. And I can go to sleep.”

Also, antiarrhythmic drugs become less effective over time, with approximately half of the patients eventually developing resistance to them.

“Pill-in-the-Pocket” Treatment

Pill-in-the-Pocket Treatment

Another treatment approach for A-Fib is to take an antiarrhythmic med at the time of an A-Fib attack.

For example, Leon writes that he takes 100 mg of flecainide three times at intervals of twenty minutes when he has an A-Fib attack. This often shortens the time of an A-Fib attack. “It (the Pill-In-The-Pocket treatment) has changed my life in that it reduces my time in A-Fib to usually a couple of hours as opposed to between 12 to 36 hours. It allows me to recover completely in a lot quicker time, because my heart hasn’t been going crazy for a day or more. And it also allows me to remain out of hospital, which has been fantastic.” (Leon, E-mail: sandman_oz (at) yahoo.com)

Marilyn writes she would take Rythmol 300 mg and Inderal 20 mg, wait three hours, then take Inderal 20 mg, wait three hours, then again start the Rythmol 300 mg and Inderal 20 mg, etc. Although she daily took a 325 mg coated aspirin, during a bout of A-Fib she would also chew an 81 mg baby aspirin. (Marilyn, E-mail: nmshook (at) sbcglobal.net)

Another treatment strategy is to take lower doses of an antiarrhythmic med on a regular basis, then take a higher dose during an A-Fib attack. A-Fib patient Reg writes he takes 300 mg of flecainide, and 2 hours later goes back into SR. He normally is on a loading dose of flecainide 100 mg in the morning and 50 mg in the afternoon. (Email: r.j.tooth (at) shu.ac.uk)

A-Fib patient Will writes that he takes Rhythmol SR 325 regularly. If he gets a break-through event of A-Fib, he takes 600 propafenone, immediate release. “This always gets me back in Sinus Rhythm, usually in 90 minutes.”

Additional Readings

Frequently Asked Questions: Drug Therapies and Medicines
Anticoagulant Therapy after Successful A-Fib Catheter Ablation: Is it Right for Me?
Warfarin vs. Pradaxa and the Other New Anticoagulants
Amiodarone: Most Effective and Most Toxic
Research Findings: Anticoagulants for Stroke Prevention
Watchman: the Alternative to Blood Thinners

Mercola, J. Over 60 Billion Doses a Year and Not ONE Death, But Still Not Safe? April 23, 2012. Last accessed April 1, 2013. URL: http://articles.mercola.com/sites/articles/archive/2012/04/23/defend-your-right-to-access-safe-dietary-supplements.aspx↵

Disclaimer: the authors of this Web site are not medical doctors and are not affiliated with any medical school or organization. The information on this site is not intended nor implied to be a substitute for professional medical advice. Always seek the advice of your physician or other qualified health professional prior to starting any new treatment or with any questions you may have regarding a medical condition. Nothing contained in this service is intended to be for medical diagnosis or treatment.